Herpes simplex virus type 1 latency in the murine nervous system is associated with oxidative damage to neurons.

Valyi-Nagy T, Olson SJ, Valyi-Nagy K, Montine TJ, Dermody TS
Virology. 2000 278 (2): 309-21

PMID: 11118355 · DOI:10.1006/viro.2000.0678

The pathological consequences of herpes simplex virus type 1 (HSV-1) latency in the nervous system are not well understood. To determine whether acute and latent HSV-1 infections of the nervous system are associated with oxidative damage, mice were inoculated with HSV-1 by the corneal route, and the extent of viral infection and oxidative damage in trigeminal ganglia and brain was assessed at 7, 90, and 220 days after inoculation. Abundant HSV-1 protein expression in the nervous system was observed in neurons and non-neuronal cells at 7 days after inoculation, consistent with viral replication and spread through the trigeminal and olfactory systems. Acute HSV-1 infection was associated with focal, neuronal and non-neuronal 4-hydroxy-2-nonenal- and 8-hydroxyguanosine-specific immunoreactivity, indicating oxidative damage. Rare HSV-1 antigen-positive cells were observed at 90 and 220 days after inoculation; however, widespread HSV-1 latency-associated transcript expression was detected, consistent with latent HSV-1 infection in the nervous system. HSV-1 latency was detected predominantly in the trigeminal ganglia, brainstem, olfactory bulbs, and temporal cortex. Latent HSV-1 infection was associated with focal chronic inflammation and consistently detectable evidence of oxidative damage involving primarily neurons. These results indicate that both acute and latent HSV-1 infections in the murine nervous system are associated with oxidative damage.

Copyright 2000 Academic Press.

MeSH Terms (17)

Animals Apoptosis Brain Brain Stem Female Herpes Simplex Herpesvirus 1, Human Inflammation In Situ Nick-End Labeling Mice Mice, Inbred BALB C Neurons Olfactory Bulb Temporal Lobe Trigeminal Ganglion Viral Plaque Assay Virus Latency

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